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The relative nephro- and neurotoxicity of colistin methanesulfonate (CMS) was investigated with rats during 7 days of intravenous administration in regimens mimicking twice- and once-daily dosing of a clinically relevant dose for humans. Histological examination revealed more-severe renal lesions with the regimen corresponding to once-daily dosing, indicating that the potential for renal toxicity may be greater with extended-interval dosing.

Colistin methanesulfonate (CMS) has the potential to hydrolyze in aqueous solution to liberate colistin, its microbiologically active and more toxic parent compound. While conversion of CMS to colistin in vivo is important for bactericidal activity, liberation of colistin during storage and/or use of pharmaceutical formulations may potentiate the toxicity of CMS. To date, there has been no information available regarding the stability of CMS in pharmaceutical preparations. Two commercial CMS formulations were investigated for stability with respect to colistin content, which was measured by a specific high-performance liquid chromatography method. Coly-Mycin M Parenteral (colistimethate lyophilized powder) was stable (<0.1% of CMS present as colistin) for at least 20 weeks at 4°C and 25°C at 60% relative humidity. When Coly-Mycin M was reconstituted with 2 ml of water to a CMS concentration of 200 mg/ml for injection, Coly-Mycin M was stable (<0.1% colistin formed) for at least 7 days at both 4°C and 25°C. When further diluted to 4 mg/ml in a glucose (5%) or saline (0.9%) infusion solution as directed, CMS hydrolyzed faster at 25°C (<4% colistin formed after 48 h) than at 4°C (0.3% colistin formed). The second formulation, CMS Solution for Inhalation (77.5 mg/ml), was stable at 4°C and 25°C for at least 12 months, as determined based on colistin content (<0.1%). This study demonstrated the concentration- and temperature-dependent hydrolysis of CMS. The information provided by this study has important implications for the formulation and clinical use of CMS products.

The acoustic effect of nasal coupling is well understood, but quantification of the extent of acoustic nasalization is difficult. This study attempts to develop an objective approach to investigate the acoustic properties of the nasals and vowel nasalization in Standard Chinese (SC). The amount of acoustic nasal coupling is quantified based on the A1-H1 (amplitude difference between the first formant and the first harmonics) and A1-P1 (amplitude difference between the first vowel formant and the nasal formant around 1000 Hz) measures. Results show that these two indices successfully distinguish between the vowels in oral and different nasal contexts. The range, rate and period of their changes provide significant information for the evaluation of nasalization.

A blind method for watermarking of 2D-vector engineering graphics
based on distance of each two adjacent vertices is proposed in this study. The
watermarking algorithm has high capacity to embed enough information for copyright
protection. Watermarks are embedded within the tolerance of the graphics, leading
to invisible distortions to the coordinates of vertices. The method is resilient
to addition/deletion entities, cropping, translation and rotation.

The role of mutations in genes for GyrA, GyrB, ParC and ParE in fluoroquinolone-resistance in Mycoplasma gallisepticum obtained in vitro and in vivo was studied. M. gallisepticum mutants were generated by stepwise selection in either 1/2xMIC or escalating concentration of enrofloxacin or ciprofloxacin. Seven fluoroquinolone-resistant clinical isolates of M. gallisepticum recovered from commercial poultry flocks with suspected chronic respiratory disease were recruited for the mutation detection of four target genes. The evolution of resistance in M. gallisepticum was more readily and more quickly with enrofloxacin selection than with ciprofloxacin selection. Selection with enrofloxacin gave mutations at GyrA83 (Ser→Ile) firstly and subsequent additional mutation at GyrA82 or GyrA103, combining substitution at ParC80 in association with high-level resistance to FQs. Selection with ciprofloxacin gave primary change at Gyr87 and subsequent additional alteration at ParC80, elevating the MICs for FQs significantly. The presence of alterations of both the GyrA and ParC in 7 clinical isolates of M. gallisepticum is in good agreement with the results from mutants selected in vitro. No mutations in GyrB and ParE were found in mutants selected both in vitro and in vivo.

Mutation in acrR would result in enhanced expression of acrAB, increasing fluoroquinolone resistance and partially contributing to the increase in resistance levels to several unrelated antibiotics. An insertion of 777 bp fragment within acrR gene was detected in a clinical E. coli isolates from a diseased duck. In order to determine whether the insertion of acrR was responsible for the elevated expression of acrAB, complementation with wild-type acrR and expression levels of efflux pump and regulator genes by qPCR were carried out. Complementation led to increased sensitivity to ciprofloxacin and to ethidium bromide and decreased expression of acrA and acrB and increased expression of global regulators marA and SoxR compared with that of the parental strains suggesting that the insertion of acrR playing important role in increased acrAB expression and ciprofloxacin resistance.

Pipeline safety is very important. A small defect in pipeline girth weld may lead to an accident. Automatic and accurate nondestructive testing method with fast detection speed is needed. Therefore, an ultrasonic phased array defect detection system has been developed. The deflection and focusing characteristics are analyzed at first. Then, detection principles based on geometrical acoustics approximation are described. And then, keys of system hardware construction and the software design are introduced. Application of this system is carried out on a weld test block of a big inch pipeline girth weld. The experiment results demonstrate the usefulness of such testing configuration and illustrate that the system can increase the testing efficiency.

Recent analyses of RNA polymerase II (Pol II) revealed that Pol II is concentrated at the promoters of many active and inactive genes. NELF causes Pol II to pause in the promoter-proximal region of the hsp70 gene in Drosophila melanogaster. In this study, genome-wide location analysis (chromatin immunoprecipitation-microarray chip [ChIP-chip] analysis) revealed that NELF is concentrated at the 5` ends of 2,111 genes in Drosophila cells. Permanganate genomic footprinting was used to determine if paused Pol II colocalized with NELF. Forty-six of 56 genes with NELF were found to have paused Pol II. Pol II pauses 30 to 50 nucleotides downstream from transcription start sites. Analysis of DNA sequences in the vicinity of paused Pol II identified a conserved DNA sequence that probably associates with TFIID but detected no evidence of RNA secondary structures or other conserved sequences that might directly control elongation. ChIP-chip experiments indicate that GAGA factor associates with 39% of the genes that have NELF. Surprisingly, NELF associates with almost one-half of the most highly expressed genes, indicating that NELF is not necessarily a repressor of gene expression. NELF-associated pausing of Pol II might be an obligatory but sometimes transient checkpoint during the transcription cycle.

A stable and low costless tunable erbium doped fiber ring laser using fiber Bragg grating-assisted add-drop filter is proposed and demonstrated. A stable laser output is obtained with a 4 nm tuning range. The power fluctuation, full-width at half maximum and SMSR are measured to be less than 0.50 dB, smaller than 0.015 nm and better than 55 dB in this tuning range.

The pollution status and horizontal distribution of heavy metals (Ni, Pb, Cr, Zn, Cu, and Cd) in the soil on railroad side along the Zhengzhou-Putian section of Longxi-Haizhou Railroad were studied by collecting soil samples along a sampling section perpendicular to the railroad at the distances of 0, 10, 20, 30, 50, 100, 200, 300, and 500 m from the railroad edge. The concentrations of heavy metals in the sampling soils were higher than those of the control site. The concentrations of Pb, Zn, and Cd were found to be the highest in the soils at the railroad edge, and then decreased with increasing distance from the railroad. The highest concentrations of Ni, Cr, and Cu in soils were located at about 10–30 m from the railroad. Compared with the single factor pollution index (SFPI) of heavy metals calculated for the control site, the average SFPI from the sampling sites decreased in the order of Cr ≥ Cd ≥ Pb ≥ Zn ≥ Ni ≥ Cu. There were notable negative correlations between the integral pollution index (IPI) of soil heavy metals at all sampling sites and the distances from the railroad. According to three IPIs calculated from the background values of heavy metals in och-aquic Cambisols, the heavy metal concentrations in the control soil, and the 2nd levels for soil heavy metals in GB15618-1995, the study area could be divided, based on the distances from the railroad, into four pollution zones: heavy pollution zone (0–10 m), medium pollution zone (10–50 m), slight pollution zone (50–100 m), and warning zone (100–500 m), respectively.

The Down syndrome candidate region 1 gene (DSCR1) can be expressed as four isoforms, one of which is the well-studied isoform 4 (DSCR1-4) that is induced by VEGF-A165 to provide a negative feedback loop in the VEGF-A165-induced angiogenesis. We reported previously that another DSCR1 isoform, DSCR1-1L, was also up-regulated by VEGF-A165 in cultured endothelial cells and in several in vivo models of pathological angiogenesis and that different from DSCR1-4, DSCR1-1L overexpression alone induced cultured endothelial cell proliferation and promoted angiogenesis in Matrigel assays. It was reported recently that tumor growth was greatly repressed in DSCR1 knock-out mice. Although DSCR1-4 transcription was primarily regulated by NFAT, the mechanism regulating DSCR1-1L expression was still unknown. We developed human DSCR1-1L promoter-driven luciferase system and found that deletion of a putative conserved M-CAT site located 1426-bp upstream of the translation start site blunted promoter activity. We further showed that knockdown of TEF3, not other members of TEF family inhibited VEGF-A165-induced DSCR1-1L expression. We also demonstrated that TEF3 directly interacted with the putative M-CAT site in the DSCR1-1L promoter in vitro and in vivo. Finally, overexpression of TEF3 isoform 1, not isoform 3, in HUVEC was sufficient to induce DSCR1-1L expression even in the absence of VEGF-A165 stimulation. Taken together, we elucidated a novel function of transcriptional factor TEF3. TEF3 was required for DSCR1-1L expression through binding to the M-CAT site in its promoter and could be an attractive target for anti-angiogenesis therapy.

The pluripotency and self-renewal of embryonic stem cells (ESC) are regulated by a variety of cytokines/growth factors with some species differences. We reported previously that rabbit ESC (rESC) are more similar to primate ESC than to mouse ESC. However, the signaling pathways that regulate rESC self-renewal had not been identified. Here we show that inhibition of the transforming growth factor β (TGFβ), fibroblast growth factor (FGF), and canonical Wnt/β-catenin (Wnt) pathways results in enhanced differentiation of rESC accompanied by down-regulation of Smad2/3 phosphorylation and β-catenin expression and up-regulation of phosphorylation of Smad1 and β-catenin. These results imply that the TGFβ, FGF, and Wnt pathways are required for rESC self-renewal. Inhibition of the MAPK/ERK and PI3K/AKT pathways, which lie downstream of the FGF pathway, led to differentiation of rESC accompanied by down-regulation of phosphorylation of ERK1/2 or AKT, respectively. Long-term self-renewal of rESC could be achieved by adding a mixture of TGFβ ligands (activin A, Nodal, or TGFβ1) plus basic FGF (bFGF) and Noggin in the absence of serum and feeder cells. Our findings also suggest that there is a regulatory network consisting of the FGF, Wnt, and TGFβ pathways that controls rESC pluripotency and self-renewal. We conclude that bFGF controls the stem cell properties of rESC both directly and indirectly through TGFβ or other pathways, whereas the effect of Wnt on rESC might be mediated by the TGFβ pathway.